HLA-C and neoplasm: The heightened occurrence of nonsynonymous SNVs and frameshift mutations generates numerous immunogenic neoantigens on the major histocompatibility complex (MHC) class I molecules on tumor cells and on MHC class I and II on antigen-presenting cells, thereby priming T cells to identify them as non-self and recruiting T cells within the tumor as TILs [11, 137, 138].